2010
DOI: 10.1016/j.jsbmb.2010.05.004
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Disruption of Pdia3 gene results in bone abnormality and affects 1α,25-dihydroxy-vitamin D3-induced rapid activation of PKC

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Cited by 42 publications
(40 citation statements)
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“…By establishing the role of Pdia3 in 1␣,25(OH) 2 D 3 -dependent gene transcription, protein secretion and mineralization, we showed that the proposed Pdia3 signaling pathway has significant physiological relevance. This conclusion is supported by studies showing that mice with reduced levels of Pdia3 (Pdia3 ϩ/Ϫ ) have a defective bone phenotype (50).…”
Section: Discussionmentioning
confidence: 77%
“…By establishing the role of Pdia3 in 1␣,25(OH) 2 D 3 -dependent gene transcription, protein secretion and mineralization, we showed that the proposed Pdia3 signaling pathway has significant physiological relevance. This conclusion is supported by studies showing that mice with reduced levels of Pdia3 (Pdia3 ϩ/Ϫ ) have a defective bone phenotype (50).…”
Section: Discussionmentioning
confidence: 77%
“…This effect is abolished in PDIA3-knockdown cells, indicating that PDIA3 mediates the 1a,25(OH) 2 D 3 membrane response [39]. The PDIA3 knockout mouse is embryonically lethal by day E10.5 [51], confirming the importance of this protein in stem cell differentiation and …”
Section: Vitamin D Receptor Expressionmentioning
confidence: 88%
“…In addition, PDIA3 deficiency in PDIA3 + / -mice results in skeletal anomalies that affect trabecular and cortical bone [51]. Interestingly, the stimulatory effect of the 1a,25(OH) 2 EBs also exhibited increased expression of mRNAs for a2 and b1 integrin subunits in cultures grown in osteogenic medium.…”
mentioning
confidence: 99%
“…However, chondrocytes isolated from costochondral cartilage of VDR knockout mice and Ca 2+ influx studies in the guts of these mice demonstrate that 1α,25(OH) 2 D 3 still elicits rapid activation of PKC and a biological response [38,39]. Studies using Pdia3 conditional knockout mice [40], Pdia3-silenced osteoblasts [41], and Pdia3 ± heterozygote mice [42] have demonstrated a loss of rapid activation of PKC and release of PGE 2 , decreased osteopontin production and alkaline phosphatase activity, and bone and cartilage abnormalities.…”
Section: Alternative Membrane Receptorsmentioning
confidence: 99%